• 1 January 1983
    • journal article
    • research article
    • Vol. 49  (4) , 705-715
Abstract
Unopsonized zymosan effectively induces a respiratory burst (O2- release, hexose monophosphate (HMP) shunt stimulation) in thioglycollate-elicited and BCG-activated [mouse] macrophages (M.vphi.). These M.vphi. express lectin-like receptors specific for mannose or fucose-terminated glycoconjugates (MFR). A role for the MFR in phagocytosis of zymosan was demonstrated by cultivating M.vphi. on a glutaraldehyde-fixed layer of zymosan, a procedure which depleted M.vphi. of MFR-mediated pinocytic activity, but not other surface antigens (F4/80, Mac-1) or receptors (FcR [Fc receptor], C3R [complement component 3 receptor]). After modulation of MFR, M.vphi. lost the ability to phagocytose zymosan, but ingested antibody or complement-coated zymosan vigorously via alternative receptors. Challenge with free zymosan failed to enhance respiratory burst activity in M.vphi. which had been cultivated on zymosan. Such M.vphi. were also refractory to zymosan taken up by alternative receptors or other ingested particles (EIgG [IgG-coated sheep erythrocyte]), but responded to a non-particulate challenge, PMA. The MFR, like other receptors, can mediate phagocytosis and elicit a respiratory burst in suitably primed M.vphi., but phagocytosis via specific receptors (FcR, C3R) need not trigger a respiratory burst.

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